ArticleThe Biochemical journal2006
Poly(ADP-ribose) glycohydrolase silencing protects against H2O2-induced cell death.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 98 citations in OpenAlex.
- Article
- Molecular mechanisms of cell death by parthanatos: More questions than answers.Genetics and molecular biology · 2024Article
- Glutamine protects mouse spermatogonial stem cells against NOX1-derived ROS for sustaining self-renewal division in vitro.Development (Cambridge, England) · 2023Article
- Article
- Transcriptional analysis of immune response genes during pathogenesis of cytomegalovirus retinitis in mice with murine acquired immunodeficiency syndrome.PLoS pathogens · 2020Article
- Parthanatos-associated proteins are stimulated intraocularly during development of experimental murine cytomegalovirus retinitis in mice with retrovirus-induced immunosuppression.Journal of medical virology · 2020Article
- New Perspectives for Resistance to PARP Inhibitors in Triple-Negative Breast Cancer.Frontiers in oncology · 2020Review
- Poly(ADP-Ribose) Glycohydrolase (PARG) vs. Poly(ADP-Ribose) Polymerase (PARP) - Function in Genome Maintenance and Relevance of Inhibitors for Anti-cancer Therapy.Frontiers in molecular biosciences · 2020Review
- Multi-targeted Effect of Nicotinamide Mononucleotide on Brain Bioenergetic Metabolism.Neurochemical research · 2019Review
- Emerging roles of eraser enzymes in the dynamic control of protein ADP-ribosylation.Nature communications · 2019Review
- Nucleolar-nucleoplasmic shuttling of TARG1 and its control by DNA damage-induced poly-ADP-ribosylation and by nucleolar transcription.Scientific reports · 2018Article
- Radiosensitization with an inhibitor of poly(ADP-ribose) glycohydrolase: A comparison with the PARP1/2/3 inhibitor olaparib.DNA repair · 2018Article
- From the Cover: ROS-Induced Store-Operated Ca2+ Entry Coupled to PARP-1 Hyperactivation Is Independent of PARG Activity in Necrotic Cell Death.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Disrupted ADP-ribose metabolism with nuclear Poly (ADP-ribose) accumulation leads to different cell death pathways in presence of hydrogen peroxide in procyclic Trypanosoma brucei.Parasites & vectors · 2016Article
- An assay to measure poly(ADP ribose) glycohydrolase (PARG) activity in cells.F1000Research · 2016Article
- PARG deficiency is neither synthetic lethal with BRCA1 nor PTEN deficiency.Cancer cell international · 2016Article
- Functional Role of ADP-Ribosyl-Acceptor Hydrolase 3 in poly(ADP-Ribose) Polymerase-1 Response to Oxidative Stress.Current protein & peptide science · 2016Review
- Poly(ADP-Ribose) Glycohydrolase (PARG) Silencing Suppresses Benzo(a)pyrene Induced Cell Transformation.PloS one · 2016Article
- Enhanced cytotoxicity in triple-negative and estrogen receptor‑positive breast adenocarcinoma cells due to inhibition of the transient receptor potential melastatin-2 channel.Oncology reports · 2015Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PAR [poly(ADP-ribose)] is a structural and regulatory component of multiprotein complexes in eukaryotic cells. PAR catabolism is accelerated under genotoxic stress conditions and this is largely attributable to the activity of a PARG (PAR glycohydrolase). To overcome the early embryonic lethality of parg-knockout mice and gain more insights into the biological functions of PARG, we used an RNA interference approach. We found that as little as 10% of PARG protein is sufficient to ensure basic cellular functions: PARG-silenced murine and human cells proliferated normally through several subculturing rounds and they were able to repair DNA damage induced by sublethal doses of H2O2. However, cell survival following treatment with higher concentrations of H2O2 (0.05-1 mM) was increased. In fact, PARG-silenced cells were more resistant than their wild-type counterparts to oxidant-induced apoptosis while exhibiting delayed PAR degradation and transient accumulation of ADP-ribose polymers longer than 15-mers at early stages of drug treatment. No difference was observed in response to the DNA alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine, suggesting a specific involvement of PARG in the cellular response to oxidative DNA damage.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.